Background:Spontaneous pneumomediastinum (SPM) is an uncommon disorder. It is rarely reported in paediatric patients and may be accompanied by subcutaneous emphysema. It is usually benign and self-limiting, with only supportive therapy being needed, but severe cases may require invasive measures. Asthma exacerbations have classically been described as a cause of SPM. However, detailed descriptions in asthmatic children are scarce. We aimed at improving the current understanding of the features of SPM and subcutaneous emphysema, and outcomes, by means of a case report and a systematic review.Methods:For the systematic review a literature search was performed in PubMed to identify reported cases of SPM in asthmatic children.Results:The case a 10-year-old asthmatic girl with SPM is reported. The patient received an inhaled corticosteroid and long-acting beta2 agonist, in addition to sublingual immunotherapy (SLIT) with eventual control of asthma symptoms. Review: A total of 114 published cases were found since 1995, most of them in teenagers; no sex differences were observed. Clinical presentation was associated with an asthma exacerbation in a number of cases. Other presenting features were chest pain, dyspnoea, cough, and particularly acute swelling of the face, neck, and upper chest. Subcutaneous emphysema was present in most patients. Overall, three cases of pneumothorax and two cases of pneumorrhachis were reported. Therapy was mainly based on supportive care, rest, oxygen therapy, analgesics, steroids, and bronchodilators. All patients recovered spontaneously, in spite of a small initial increase in SPM in a few cases.Conclusions:Early identification of patients at risk of SPM would avoid the high number of under-diagnosed cases. Patients should be treated not only with supportive therapy but also with measures to achieve control of the underlying cause (such as poorly controlled asthma).

a b s t r a c tThe deleterious effects of oxidants on proteins may be modified by overexpression of uncoupling protein 3 (UCP3) in skeletal muscle cells exposed to hyperoxia or H 2 O 2 . UCP3 overexpression significantly attenuated the increase in protein carbonylation in response to hyperoxia and H 2 O 2 exposures. However, antioxidant enzyme content and activity (superoxide dismutases, peroxiredoxins, glutathione peroxidase-I, and catalase) were reduced or not modified in UCP3-overexpressing myotubes exposed to oxidants. Protein nitration increased in UCP3-overexpressing cells exposed to hyperoxia, but not to H 2 O 2 . We conclude that protein oxidation rather than nitration is neutralized by UPC3 overexpression in mouse myotubes exposed to abundant reactive oxygen species.

In severe COPD patients, oxidative stress, which is involved in their peripheral muscle dysfunction, increases in response to exercise. In this study, muscle oxidative stress was explored after quadriceps magnetic stimulation training. A randomized controlled study was conducted on very severe COPD patients, who underwent quadriceps magnetic stimulation training for 8 weeks. A control group was also studied. In both groups, vastus lateralis specimens were obtained before and after the 8-week period. Muscle protein carbonylation and nitration and antioxidant enzymes were determined using immunoblotting and proportions and sizes of type I and II fibres using immunohistochemistry. Compared to controls, magnetic stimulation muscle training did not modify redox balance, whilst inducing a significant increase in type I fibre sizes. In severe COPD patients, it is concluded that quadriceps magnetic stimulation training was a well-tolerated therapeutic intervention, which did not enhance muscle oxidative stress, while increasing the size of slow-twitch fibres.

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Introduction Stroke and transient ischemic attack (TIA) are important periprocedural cerebrovascular complications of transcatheter aortic valve implantation (TAVI). Regional cerebral O2 saturation is an indicator for cerebral perfusion and can be measured in real-time and noninvasively by near-infrared spectroscopy (NIRS). In this pilot study we evaluated the feasibility and utility of NIRS during TAVI. Methods Regional cerebral O2 saturation (rScO2, bihemispheric) was measured by near-infrared spectroscopy during 32 transfemoral TAVI procedures (female 56.3%, mean age 81.8 years). All patients received conscious sedation and O2-supplement if peripheral oxygen saturation (SpO2) was below 95%. Baseline rScO2 was measured at the beginning of the procedure, as well as before, during and 5min after rapid pacing for valve deployment. Results Mean preoperative mini mental state examination score was 26.5 points (theoretically max. 30 points, >24 points no severe cognitive impairment). Two-third of the patients (n=21) required oxygen supply (mean 4.0 l/min) during the TAVI procedure. Mean baseline rScO2 was 59.3% with no differences between both cerebral hemispheres (left 60.3% vs. right 58.7% p=0.23). Compared to baseline rScO2 and rScO2 assessed immediately before rapid passing, rScO2 dropped significantly during rapid pacing (59.3% vs. 51.8%, p<0.01 and 60.9% vs. 51.8%, p<0.01 respectively). Five minutes after rapid pacing rScO2 values had normalized again (post rapid pacing 60.9% vs. 51.8% during rapid pacing, p<0.01; baseline 59.3% vs. post rapid pacing 60.9%, p=0.51). Intraprocedural cerebrovascular events were observed in two cases. One patient developed a left-sided hemiplegia (stroke, later verified by cerebral CT scan) and one patient a transient tremor of the left upper extremity (TIA, new hemorrhagic or ischemic event ruled out by cerebral CT scan). In both cases we observed an abnormal sudden rScO2 decrement by the corresponding right hemispheric NIRS sensor (left-right hemisphere sensor: 60% vs. 44% and 63% vs. 48% respectively). Conclusion Regional cerebral O2 saturation, an indicator for cerebral perfusion, decreases significantly during rapid pacing of TAVI procedure. Furthermore, rScO2 measurement by NIRS may be helpful to detect cerebrovascular complications early during TAVI procedure.

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